We have completed and published the first Phase I study of recombinant LCAT showing that it was safe and raised HDL-C. In addition we published the first enzyme replacement therapy of LCAT in a patient with Familial LCAT Deficiency, showing that it normalized their lipoprotein profile. We also completed and published a study showing that LpX, the abnormal lipoprotein particle that accumulates in LCAT Deficiency, causes renal disease in an animal model. Recently we have developed an mouse model for LCAT deficiency that form high levels of LpX and spontaneously develop renal disease and showed that recombinant LCAT prevents renal disease. These finding supports the future use of LpX as a potential biomarker for monitoring rLCAT therapy and are working with MedImmune under a CRADA for further development of rLCAT.